Purpose of review Anemia
is prevalent in patients with infections and other inflammatory conditions. Induction of the iron
regulatory hormone hepcidin
has been implicated in the pathogenesis of anemia
. This review outlines recent discoveries in understanding how hepcidin
and its receptor ferroportin
are regulated, how they contribute to anemia
, and how this knowledge may help guide new diagnostic and therapeutic strategies for this disease.
IL-6 is a primary driver for hepcidin
induction in many models of anemia
, but the SMAD1/5/8 pathway also contributes, likely via Activin B and SMAD-STAT3 interactions at the hepcidin
has an important functional role in many, but not all forms of anemia
, although hepcidin
-independent mechanisms also contribute. In certain populations, hepcidin
assays may help target therapy with iron
or erythropoiesis-stimulating agents to patients who may benefit most. New therapies targeting the hepcidin
axis have shown efficacy in preclinical and early clinical studies.
Recent studies confirm an important role for the hepcidin
axis in the development of anemia
, but also highlight the diverse and complex pathogenesis of this disorder depending on the underlying disease. Hepcidin
-based diagnostic and therapeutic strategies offer promise to improve anemia
treatment, but more work is needed in this area.